Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The density of bone in the distal third of the radius was measured in 13 men and 17 women with primary hyperparathyroidism. The bone density was significantly reduced (as compared to age-matched controls) in 7 of 11 postmenopausal women. However, it was reduced in only 2 of 13 men and in 1 of 6 premenopausal women. Thus, most of the postmenopausal women with primary hyperparathyroidism had low bone density, whereas most men and premenopausal women with this condition had normal bone density. The results support the conclusion that oestrogen deficiency may contribute to the development of bone disease by sensitising bone to the action of parathyroid hormone.
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PMID:Photon absorptiometric analysis of bone density in primary hyperparathyroidism. 4 47

Plasma concentrations of calcium, phosphate, alkaline phosphatase (A.P.), immunoreactive calcitonin (iC.T.), and immunoreactive parathyroid hormone (iP.T.H.) were measured in fifty-two patients with chronic renal failure on maintenance haemodialysis. On the basis of a bimodal distribution of values for plasma-A.P. the patients were dividied into 2 groups. In those patients with normal A.P. concentratons as well as in twenty-eight normal subjects there was a positive correlation between iP.T.H. and iC.T. which was independent of plasma calcium or phosphate. Patients with increased plasma-A.P. had higher concentrations of iP.T.H., lower concentrations of iC.T., and showed a negative relation between the concentrations of the two hormones. It is suggested that a possible factor in the pathogenesis of renal bone disease is a failure to secrete C.T. in adequate amounts.
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PMID:Evidence that endogenous calcitonin protects against renal bone disease. 6 2

Biochemical and bone morphometric measurements were evaluated in 12 patients who were on long-term anticonvulsant therapy with barbiturates. Half of the patients had no symptomatic bone disease, and half presented with bone disease and pain. Serum biochemical values were normal except for a few patients who had an elevated serum level of parathyroid hormone; the concentration of serum 25-hydroxy vitamin D was decreased in the majority of patients in whom it was measured. Bone absorptiometric values were normal but proved to be misleading: the Singh Index and videodensitometric measurements indicated that bone mass was below normal in all patients. Bone morphometric data indicated that bone resorption was 3 times greater than normal, and there was no evidence of osteomalacia. Vitamin D and possibly calcium have been suggested as potentially useful agents in the treatment of the bone disease associated with chronic anticonvulsant therapy.
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PMID:The frequency of bone abnormality in patients on anticonvulsant therapy. 7 73

Hypercalcemia is very uncommon in small cell (oat cell) carcinoma of the lung. Two cases of this neoplasm associated with symptomatic hypercalcemia are described. Despite normal skeletal roentgenograms, metastatic bone disease was demonstrated by abnormal bone scans and bone biopsies in both patients. The combination of conventional antihypercalcemia therapy, cytotoxic cancer chemotherapy, and synthetic salmon calcitonin corrected the hypercalcemia despite progression of the small cell carcinoma. One patient with elevated serum immunoreactive parathyroid hormone (PTH) had a parathyroid adenoma at autopsy. This association emphasizes that in cases of bronchogenic small cell carcinoma with hypercalcemia, conincidental primary hyperparathyroidism should be considered.
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PMID:Hypercalcemia in small cell (oat cell) carcinoma of the lung. Coincident parathyroid adenoma in one case. 17 Oct 50

Effects of parathyroidectomy on parathyroid function and calcium (Ca) metabolism were carefully evaluated in 6 patients with primary hyperparathyroidism without symptoms normally attributed to the disease and in 7 with bone disease or nephrolithiasis. Before parathyroidectomy, both groups of patients demonstrated evidence of the sequelae of parathyroid hormone (PTH) excess, since they presented one or more of the following features: low bone density by 125I-photon absorption, hypercalciuria (urinary Ca greater than 200 mg/day on an intake of 400 mg/day), negative Ca balance (absorbed Ca less than urinary Ca), elevated fasting urinary Ca greater than 0.2 mg/mg creatinine for a night-time sample after a 6-hour fast), and decreased renal function (creatinine clearance of less than 65 ml/min). Following parathyroidectomy, most of these deleterious effects were reversed commensurate with the return of immunoreactive serum PTH, serum Ca, and urinary cyclic AMP toward normal. These quantitative non-invasive techniques may be useful for the initial evaluation and follow-up of patients with asymptomatic primary hyperparathyroidism.
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PMID:Metabolic effects of parathyroidectomy in asymptomatic primary hyperparathyroidism. 17 69

There has been much progress in our understanding of the metabolism of vitamin D. It is now clear that vitamin D3 can be produced in the skin or ingested in the diet. It accumulates very rapidly in the liver where it undergoes 25-hydroxylation, yielding 25-OH-D3, the major circulating metabolite of the vitamin. 25-OH-D3 proceeds to the kidney where it undergoes one of two hydroxylations. If there is a biological need for calcium or for phosphate the kidney is stimulated to convert 25-OH-D3 to the 1,25-(OH)2-D3, a calcium and phosphate mobilizing hormone. If, however, the animal has sufficient supplies of calcium and phosphate, the l-hydroxylase is shut down and instead the 25-OH-D3 is converted to a 24,25-(OH)2D3. The role of the 24,25-(OH)2D3 remains unknown; it may be an intermediate in the inactivation-excretion mechanism. 1,25-(OH)2D3 proceeds to the intestine where it stimulates intestinal calcium transport and intestinal phosphate transport. It also stimulates bone calcium mobilization and probably has other effects yet to be discovered in such tissues as muscle. The 25-OH-D3-l-hydroxylase, which is located exclusively in renal mitochondria, has been shown to be a three component system involving a flavoprotein, an iron-sulfur protein (renal ferredoxin), and a cytochrome P-450. This system has been successfully solubilized, the components isolated, and reconstituted. The 24-hydroxylase, however, has not yet been thoroughly studied. 1,25-(OH)2D3 is necessary for the appearance of the 24-hydroxylase; parathyroid hormone represses 24-hydroxylation. It is possible that the 24-hydroxylase represents the major regulated enzyme, so that its presence or absence may determine whether 1,25-(OH)2D3 is produced. Two metabolic pathways for 1,25-(OH)2D3 are known, conversion by the 24-hydroxylase to 1,24,25-(OH)3D3, and conversion of 1,25-(OH)2D3 to an unknown substance. In the latter instance, there occurs loss of a side chain piece, including at least one of the 26 and 27 carbons. Whether 1,25-(OH)2D3 must be metabolized further before it carries out all of its functions has yet to be established. The primary excretion route of vitamin D3 is via the bile into the feces. Urinary excretion appears small in magnitude and no excretion products have yet been identified positively. Much remains to be learned concerning the metabolism and function of vitamin D and its metabolites. This should therefore, prove to be a fruitful area of investigation for many years to come, especially since 1,25-(OH)2D3, 25-OH-D3, and lalpha-OH-D3 have been shown to be effective in a number of metabolic bone disease states.
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PMID:Metabolism of vitamin D: current status. 18 53

1,25 dihydroxycholecalciferol [1,25(OH)2D3] was studied in a double-blind controlled fashion in patients on chronic dialysis. Serum calcium was unchanged in 16 patients on vitamin D3 (D3) (400 to 1200 IU/day). In 15 patients on 1,25(OH)2D3 (0.5 to 1.5 microgram/day), serum calcium increased from 9.05 +/- .15 to 10.25 +/- .20 mg/dl (p less than 0.001), returning to 9.37 +/- .16 mg/dl (p less than 0.001) in the post control period. Patients on D3 showed no reversible decrease in immunoreactive parathyroid hormone levels, but patients on 1,25(OH)2D3 did, from a control of 1077 +/- 258 to 595 +/- 213 microliter equivalents/ml (p less than 0.01), and returned to 1165 +/- 271 microliter equivalents/ml (p less than 0.005). Nine of 12 patients on D3 who underwent serial iliac-crest biopsies showed histologic deterioration, and six of seven who received 1,25(OH)2D3 were improved or unchanged (p less than 0.025). Bone mineral and calcium decreased in patients on D3 (p less than 0.05) but not in those on 1,25(OH)2D3. Hypercalcemia occurred in five of 15 patients. We conclude that 1,25(OH)2D3 has a calcemic effect in chronic dialysis patients, decreases levels of immunoreactive parathyroid hormone, and is associated with histologic improvement in bone disease. Thus, 1,25(OH)2D3 is a valuable adjunct to the management of renal osteodystrophy but requires monitoring of serum calcium to avoid hypercalcemia.
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PMID:1,25 dihydroxycholecalciferol effects in chronic dialysis. A double-blind controlled study. 20 39

A female pet wooly monkey with metabolic bone disease initially presented with a proliferating bony mass in the left humerus which had many features of osteosarcoma. At necropsy, parathyroid hyperplasia, osteoclastic resorption, proliferative osteoid deposition in the calvarium and cortex of long bones, and fibrous proliferation of the marrow indicated the presence of generalized osteodystrophia fibrosa. The dietary history of deficient vitamin D3 and protein and minimal exposure to sunlight supported this diagnosis, as did depressed levels of serum calcium and elevated levels of serum parathyroid hormone, alkaline phosphatase, and acid phosphatase.
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PMID:Metabolic bone disease resembling osteosarcoma in a wooly monkey (Lagothrix lagotricha). 21 39

Calcium and vitamin D metabolism were evaluated in 5 adult epileptic patients before and during treatment with phenytoin. Significant decreases occurred in serum concentrations of calcium, albumin, and 25-hydroxy-cholecalciferol. The decreases in serum calcium paralleled those in serum albumin. Significant increases occurred in serum alkaline phosphatase and 1 alpha, 25-dihydroxycholecalciferol, in urinary hydroxyproline, and in the fractional gastrointestinal absorption of calcium. Urinary cyclic adenosine monophosphate and serum parathyroid hormone did not change. The results suggest that the bone disease resulting from phenytoin therapy may be associated with a deficiency of 25-hydroxycholecalciferol and not of 1 alpha, 25-dihydroxycholecalciferol, and that reduced gastrointestinal absorption of calcium or changes in parathyroid function may not be necessary for the development of bone disease.
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PMID:Effect of phenytoin on bone and vitamin D metabolism. 22 Sep 3

The discovery of the vitamin D endocrine system has opened up many possibilities in our understanding of metabolic bone disease. Of particular importance is the fact that we can now manage certain genetic disorders resulting in vitamin D-resistant rickets or vitamin D-resistant hypocalcemia with the new active hormonal forms of vitamin D and with intelligent dietary management to provide for correction of the mineral difficulty. Thus, in the case of vitamin D dependency, replacement need only be with the missing hormone, 1,25-(OH)2D3. On the other hand, familial hypophosphatemia requires adjustment of the plasma phosphorus by frequent administration of oral phosphate and the adjustment of intestinal calcium absorption by 1,25-(OH)2D3. Renal failure patients require the adjustment of plasma phosphorus concentration and parathyroid hormone status, and the administration of the missing hormone 1,25-(OH)2D3. Hypoparathyroid patients require oral calcium plus 1,25-(OH)2D3, and premature infants require administration of the 1,25-(OH)2D3 because the immature kidneys and immature parathyroid glands fail to produce the required amount of this hormone. Other vitamin D-resistant rachitic conditions cannot be discussed here for lack of space and for lack of information. Undoubtedly, such patients as those having rickets secondary to renal tubular acidosis and rickets secondary to hepatic disorders will eventually come under effecti dietary and hormonal management. In this sense, the vitamin D endocrine system and vitamin D-resistant rickets can serve as a prototype of management of a genetic disorder by dietary means.
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PMID:Vitamin D-resistant rickets. A prototype of nutritional management of a genetic disorder. 23 Sep 41


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